Iranian researchers assigned type 2 diabetics to broccoli sprout powder or placebo.
Broccoli sprout powder appears to be a useful food ingredient for improving cholesterol levels in type 2 diabetes patients, according to a recent human clinical trial.
Researchers from Shahid Beheshti University of Medical Sciences in Tehran, Iran assigned 72 men and women with type 2 diabetes to consume 10 g of broccoli powder, 5 g of broccoli powder, or placebo daily for four weeks.
After the full round of supplementation, the high dose of broccoli sprout powder was associated with significantly increased HDL cholesterol, significantly decreased serum triglycerides, and a healthier ratio of oxidized LDL cholesterol-to-LDL cholesterol, compared to a lesser dose of powder or placebo. Oxidized LDL cholesterol is understood for its potential to accelerate heart disease.
HDL cholesterol and a common predictor of atherosclerosis (Atherogenic Index of Plasma) also saw improvements with the high dose of broccoli sprout powder.
The Iranian study on broccoli sprout powder is now published in the journal Diabetes Research and Clinical Practice.
In another study on type 2 diabetes patients, the same researchers linked consumption of broccoli sprout powder with decreased oxidized LDL cholesterol, decreased malondialdehyde (a biomarker of oxidative stress), and increased total antioxidant levels.
Meta-analysis does not find increased risk of bleeding events from omega-3 PUFA consumption
July 8th 2024Researchers reviewed 11 studies and found that there was no difference in the incidence of bleeding events between patients receiving omega-3 PUFAs and those not receiving them. High dose EPA consumption was associated with an elevated but modest risk.
Recent review states that pentadecanoic acid may support cellular stability for better longevity
June 25th 2024According to the paper’s author, Stephanie Venn-Watson, DVM, MPH, deficiency in pentadecanoic acid of ≤0.2% total circulating fatty acids increases the risk of ferroptosis, which a type of cell death cause by the peroxidation of fragile fatty acids in cell membranes that combines with iron thus increasing reactive oxygen species, and disabling mitochondria.